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. Author manuscript; available in PMC: 2011 May 1.
Published in final edited form as: J Neurochem. 2010 Feb 1;113(3):649–660. doi: 10.1111/j.1471-4159.2010.06622.x

Figure 5.

Figure 5

NA uses both receptor-dependent and independent signaling to inhibit cell death pathways. A. β-adrenoceptor antagonists CGP and ICI (10 μM each) failed to block 10 μM NA protection of hNT neurons against ROS induced by 1 hour of 10 μM Aβ25–35 exposure. *, p < 0.01 vs. CTL. On the other hand, CGP and ICI pretreatment did inhibit NA’s ability to block Aβ-mediated mitochondrial membrane depolarization (B) and caspase activation (C) after 24 hours. *, p < 0.01 vs. CTL; **, p < 0.01 vs. Aβ; #, p < 0.05 vs. NA; n = 4/treatment group in 3 independent experiments.